About
Tobacco use remains the single most preventable cause of disease, disability, and death in the United States and in California. The Tobacco-Related Disease Research Program (TRDRP) is one of three entities that constitute California’s program to control tobacco consumption and alleviate the burden of tobacco-related disease. This effort was initiated by Proposition 99, “The Tobacco Tax and Health Protection Act of 1988” which mandated that the Department of Health Services, the Department of Education and the University of California be allocated a portion of the tobacco tax revenue collected to address issues of tobacco consumption and its consequences in the state. Enabling legislation requested that the University of California, in its role as the research arm of the state, “administer a comprehensive grant program to support research efforts related to the prevention, causes, and treatment of tobacco-related diseases” and that “ all qualified investigators, regardless of institutional affiliation, shall have equal access and opportunity to compete for the funds.”
The TRDRP is administered by the University of California and is a program of the Research Grants Program Office (RGPO), Office of Research and Graduate Studies at the University of California, Office of the President.
Tobacco-Related Disease Research Program
Tobacco-Related Disease Research Program Funded Publications (858)
Substance Use Among Young Adult Survivors of Childhood Cancer With Cognitive Impairment: An Analysis of the Project Forward Cohort
Purpose
Young adult childhood cancer survivors (YACCSs) are often impacted by cancer-related cognitive impairment (CRCI) and psychological distress. Using the Project Forward Cohort, we evaluated the relationship between CRCI and substance use behaviors.Methods
YACCSs were surveyed between 2015 and 2018 (N = 1,106, female = 50.8%, Hispanic = 51.5%, median age = 25.5 years). Associations between CRCI and substance use (tobacco, binge drinking, marijuana, prescription drug misuse, and e-cigarette/vaporizer) were examined in multivariate logistic or log-binomial regressions, adjusting for child at diagnosis (0-14 years), years since diagnosis, sex, race/ethnicity, cancer type, and treatment intensity. Mediation analysis was performed to determine opportunities for interventions.Results
CRCI was reported by 144 (13.0%) survivors. The highest prevalence was observed in CNS cancers (25.4%) and leukemia (13.3%) survivors. After covariate adjustment, CRCI was associated with 2.26 times the odds of prior 30-day vaping (95% CI, 1.24 to 4.11; P = .007). Mediators with significant indirect effects in the CRCI-vaping relationship include depressive symptoms (Center for Epidemiological Studies Depression Scale) and having two or more cancer-related late effects (P < .05).Conclusion
CRCI among YACCSs was associated with reports of vaping. Oncologists should screen for vaping behavior if CRCI is apparent. Increasing access to long-term follow-up clinics, addressing physical and mental health issues, and monitoring and educating on vaping and other substance use behaviors is recommended to improve the long-term health of YACCSs.Activation of the “Splenocardiac Axis” by electronic and tobacco cigarettes in otherwise healthy young adults
The "Splenocardiac Axis" describes an inflammatory signaling network underlying acute cardiac ischemia, characterized by sympathetic nerve stimulation of hematopoietic tissues, such as the bone marrow and spleen, which then release proinflammatory monocytes that populate atherosclerotic plaques, thereby promoting ischemic heart disease. Electronic (e) cigarettes, like tobacco cigarettes trigger sympathetic nerve activation, but virtually nothing is known about their influence on hematopoietic and vascular tissues and cardiovascular risks. The objective of this study was to determine if the Splenocardiac Axis is activated in young adults who habitually use either tobacco or e-cigarettes. In otherwise healthy humans who habitually use tobacco cigarettes or e-cigarettes (not both), we used 18F-flurorodeoxyglucose positron emission tomography/computer tomography (FDG-PET/CT) to test the hypothesis that tobacco or e-cigarettes increased metabolic activity of the hematopoietic and vascular tissues. FDG uptake in the spleen increased from nonuser controls (1.62 ± 0.07), to the e-cigarette users (1.73 ± 0.04), and was highest in tobacco cigarette smokers (1.82 ± 0.09; monotone P = 0.05). Similarly, FDG uptake in the aorta increased from the nonuser controls (1.87 ± 0.07) to the e-cigarette users (1.98 ± 0.07), and was highest in tobacco cigarette smokers (2.10 ± 0.07; monotone P = 0.04). FDG uptake in the skeletal muscle, which served as a control tissue, was not different between the groups. In conclusion, these findings are consistent with activation of the Splenocardiac Axis by emissions from tobacco cigarettes and e-cigarettes. This activation suggests a mechanism by which tobacco cigarettes, and potentially e-cigarettes, may lead to increased risk of future cardiovascular events.
Video-based kinetic analysis of calcification in live osteogenic human embryonic stem cell cultures reveals the developmentally toxic effect of Snus tobacco extract
Epidemiological studies suggest tobacco consumption as a probable environmental factor for a variety of congenital anomalies, including low bone mass and increased fracture risk. Despite intensive public health initiatives to publicize the detrimental effects of tobacco use during pregnancy, approximately 10-20% of women in the United States still consume tobacco during pregnancy, some opting for so-called harm-reduction tobacco. These include Snus, a type of orally-consumed yet spit-free chewing tobacco, which is purported to expose users to fewer harmful chemicals. Concerns remain from a developmental health perspective since Snus has not reduced overall health risk to consumers and virtually nothing is known about whether skeletal problems from intrauterine exposure arise in the embryo. Utilizing a newly developed video-based calcification assay we determined that extracts from Snus tobacco hindered calcification of osteoblasts derived from pluripotent stem cells early on in their differentiation. Nicotine, a major component of tobacco products, had no measurable effect in the tested concentration range. However, through the extraction of video data, we determined that the tobacco-specific nitrosamine N'-nitrosonornicotine caused a reduction in calcification with similar kinetics as the complete Snus extract. From measurements of actual nitrosamine concentrations in Snus tobacco extract we furthermore conclude that N'-nitrosonornicotine has the potential to be a major trigger of developmental osteotoxicity caused by Snus tobacco.